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Obesity, now an epidemic in the USA, northern Europe, and Italy, is associated with several co-morbidities that shorten life expectancy, in particular type 2 diabetes mellitus (T2DM), arterial hypertension, and hyperlipidemia. The impact of obesity on mortality is evident in all ages, and is especially strong in young persons. Obesity, especially visceral obesity, associated with a sedentary lifestyle, is among the strongest risk factors for T2DM, and a diagnosis of T2DM seems to increase linearly as a function of duration of obesity. The pathogenesis of T2DM is based on a dual defect, i.e. increased insulin resistance coupled with defective insulin release. The main abnormality in obesity is increased insulin resistance, while insulin release, even though defective compared with body needs, is usually abundant. The incidence of obesity among children aged 6-16 years is now even greater than that among adults: in Italy, figures up to 30% have been reported. As in adults, obesity is a cause, among children, of arterial hypertension, left ventricular hypertrophy, hyperlipidemia, non-alcoholic-steato hepatitis, sleep apnea syndrome (SAS), and orthopedic, psychological, and social problems. Together with an increase in body weight, there is an increase of visceral fat. Obesity in children has also led to a tremendous increase in the prevalence of impaired glucose tolerance (IGT); the percentages span from 25% in a multiethnic cohort in the USA, to 4% in Italian Caucasians. Management of obesity and of T2DM in children has to face the issue of poor compliance; there is consensus that dietary treatment of obese T2DM children is a failure, so that drugs are required; the only drug evaluated in a formal trial is metformin, that behaves in terms of efficacy and of minor side effects as in adults. In conclusion, obesity in children is not pure obesity, but is accompanied by co-morbidities that cluster to form the "metabolic syndrome" just like in the adults. If this epidemics continues and is not properly challenged, in the next decades we will face an epidemic of early cardiovascular morbidity and mortality.
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PMID:Type 2 diabetes mellitus is becoming the most common type of diabetes in school children. 1566 74

Obesity is becoming a global epidemic in both children and adults. It is associated with numerous comorbidities such as cardiovascular diseases (CVD), type 2 diabetes, hypertension, certain cancers, and sleep apnea/sleep-disordered breathing. In fact, obesity is an independent risk factor for CVD, and CVD risks have also been documented in obese children. Obesity is associated with an increased risk of morbidity and mortality as well as reduced life expectancy. Health service use and medical costs associated with obesity and related diseases have risen dramatically and are expected to continue to rise. Besides an altered metabolic profile, a variety of adaptations/alterations in cardiac structure and function occur in the individual as adipose tissue accumulates in excess amounts, even in the absence of comorbidities. Hence, obesity may affect the heart through its influence on known risk factors such as dyslipidemia, hypertension, glucose intolerance, inflammatory markers, obstructive sleep apnea/hypoventilation, and the prothrombotic state, in addition to as-yet-unrecognized mechanisms. On the whole, overweight and obesity predispose to or are associated with numerous cardiac complications such as coronary heart disease, heart failure, and sudden death because of their impact on the cardiovascular system. The pathophysiology of these entities that are linked to obesity will be discussed. However, the cardiovascular clinical evaluation of obese patients may be limited because of the morphology of the individual. In this statement, we review the available evidence of the impact of obesity on CVD with emphasis on the evaluation of cardiac structure and function in obese patients and the effect of weight loss on the cardiovascular system.
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PMID:Obesity and cardiovascular disease: pathophysiology, evaluation, and effect of weight loss: an update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. 1638 May 42

Polycystic ovary syndrome (PCOS) is a syndrome, which can be defined as a group of recognisable patterns of symptoms or abnormalities that indicate a particular medical situation. The current definition of PCOS requires the presence of two of the following three conditions: (i) oligo- and/or anovulation; (ii) clinical and/or biochemical signs of hyperandrogenism; and (iii) polycystic ovaries--and the exclusion of other aetiologies. It is generally accepted that the prevalence of PCOS is approximately 5-10%, and that of polycystic ovaries alone is 21-23%. Other features of PCOS are obesity, insulin resistance, impaired glucose tolerance and type 2 diabetes mellitus, dyslipidaemia, cardiovascular disease, obstructive sleep apnoea and infertility. An approach to a patient with possible PCOS should be directed towards making a diagnosis and screening for associated endocrine abnormalities. Therapeutic interventions are directed towards addressing the needs of the patient at present and towards preventing long-term complications of the syndrome. Body mass index, which is a primary mediator in the relationship between PCOS and health-related quality of life in obese PCOS adolescents, may play a similar role in other PCOS patients. Any intervention directed at reducing central obesity will not only improve quality of life but also correct hyperinsulinism and improve fertility and lipid and androgen profiles. It is also the only currently available intervention that can have a lifelong impact on reducing possible long-term complications of the syndrome. Lifestyle modification is the cardinal intervention. Pharmacological treatments are available for specific indications. Infertility can be treated with clomifene (clomiphene citrate), metformin, gonadotropins or surgery to the ovaries. Cyproterone (alone or in combination with ethinylestradiol) and spironolactone are the main drugs used in the treatment of hirsutism. Other drugs that can be considered include flutamide, ketoconazole and finasteride. Women with PCOS require ongoing surveillance to detect impaired glucose tolerance, hyperlipidaemia, endometrial hyperplasia and consequent complications. Obese women, in particular, require regular glucose tolerance testing because of the potential for rapid progression from normal to impaired glucose tolerance and diabetes. The focus of this article is the epidemiology, diagnosis and management of this common endocrine disorder. Diagnostic and co-morbid features are discussed separately to facilitate understanding of PCOS. Symptom-directed strategies, as well as short- and long-term goals of treatment, are outlined.
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PMID:Diagnosis and management of polycystic ovary syndrome: a practical guide. 1674 5

Maternal pregravid obesity is a significant risk factor for adverse outcomes during pregnancy. In early pregnancy there is an increased risk of spontaneous abortion and congenital anomalies. In later gestation maternal metabolic manifestations of the metabolic syndrome, such as gestational hypertensive disorders and diabetes, become clinically recognized because of the increased insulin resistance in obese compared with nonobese women. In women with pregestational glucose intolerance, hypertension, central obesity, and lipid disorders, the physiologic changes in pregnancy increase the risk of problems previously not routinely encountered during pregnancy. These include chronic cardiac dysfunction, proteinuria, sleep apnea, and nonalcoholic fatty liver disease. At parturition the obese patient is at an increased risk of cesarean delivery and associated complications of anesthesia, wound disruption, infection, and deep venous thrombophlebitis. For the fetus there are short-term risks of fetal macrosomia, more specifically obesity, and long-term risks of adolescent components of the metabolic syndrome. Although preliminary results of bariatric surgery are encouraging, the procedure is expensive and not for all obese women, and we recognize that long-term follow-up data on offspring of obese women who have undergone bariatric surgery before pregnancy are lacking. In the interim, we need to encourage obese women to lose weight before conception, using lifestyle changes if possible. During pregnancy, weight gain should be limited to Institute of Medicine guidelines (currently under review) and encouragement given for physical activity.
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PMID:Management of obesity in pregnancy. 1726 45

Polycystic ovaries syndrome (PCOS) is one of the most common female hormonal disorders. Its multiple components--reproductive, metabolic, neoplasic and cardiovascular--have a major impact on the public health. Androgen excess and resistance to insulin, probably from genetic origin, are responsible for most of the clinical symptomatology. Resistance to insulin seems to be accompanied by a greater risk of glucose intolerance, type 2 diabetes, lipidic anomalies and can involve the development of cardiovascular diseases. In addition, sleep apnea syndrome is more progressively described in PCOS. Infertility, menses disorders and hirsutism often push these patients to consult their physician. A better understanding of the physiopathological mechanisms led to the emergence of new therapeutic options increasing the sensitivity to insulin. Besides the pregnancy wishes, cares aim to attenuate the marks of the hyper-androgenism (hormonal treatment and cosmetic) and to correct cardiovascular, respiratory and gynaecological risk factors. In case of infertility by anovulation, cares must be performed by trained experts to minimize the risk of ovarian hyper-stimulation syndrome and multiple pregnancies. A gradation from loose weight to clomiphene citrate ovulation induction, ovarian drilling, low dose gonadotropin, in vitro fertilisation, or in vitro maturation of oocytes should bring back good reproduction potential.
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PMID:[Polycystic ovary syndrome (PCOS)]. 1754 May 11

It is estimated that 60%-7% of women of reproductive age have polycystic ovarian syndrome (PCOS). Women with this condition exhibit an adverse cardiovascular risk profile, characteristic of the cardiometabolic syndrome and given the high prevalence of PCOS in the female population, this condition may contribute towards the acceleration of cardiovascular disease among young women. This article summarizes the recent development and findings in the cardiometabolic abnormalities in patients with PCOS. Patients with PCOS have the clinical features of oligomenorrhoea, hirsutism and infertility; however, they also exhibit hyperinsulinemia, obesity, hypertension, dyslipidemia, and an increased pro-thrombotic state. They have an increased risk of type 2 diabetes and impaired glucose tolerance, and sleep apnea is also found more commonly in this population. However, despite the presence of cardiovascular risk factors and increased surrogate markers of cardiovascular disease it is unclear if they have accelerated atherosclerosis. End point studies are currently lacking and the available evidence are conflicting. Adipose tissue has emerged as an important endocrine organ over the last decade and gained recognition in having an important role in the cardiometabolic syndrome. Adiponectin that is secreted exclusively by adipocytes has recently been recognized as an important marker of cardiometabolic syndrome, obesity, type 2 diabetes, and coronary artery disease. Other adipocytokines like leptin and resistin have also recently been recognized. This article will address the current evidence for the adverse cardiovascular risk in PCOS and the other factors that may be implicated. Finally the therapeutic options for treatment will be discussed.
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PMID:Cardiometabolic aspects of polycystic ovarian syndrome. 1758 75

In this study of obstructive sleep apnoea (OSA), glucose tolerance and liver steatosis in females from an obesity unit, 45 patients (mean age 46.8 years, mean body mass index 39.4 kg/m(2), all non-diabetic and alcohol abstainers) underwent nocturnal polysomnography, a 2 h oral glucose tolerance test and abdominal ultrasonography. OSA, defined as an apnoea-hypopnoea index (AHI) of > or = 10 events/h, was present in 20 patients (44%). Impaired glucose tolerance (IGT) was found in eight patients (40%) with OSA and three patients (12%) without OSA; there was a positive linear relationship between AHI and post-load glucose levels. On multivariate logistic regression analysis, IGT was predicted by OSA independently of age, waist circumference, systolic blood pressure and current smoking. Liver steatosis was present in 37 women (82.2%), of whom six had grade III steatosis. Of the variables tested, IGT was the only predictor of grade III steatosis. In conclusion, OSA is an independent predictor of IGT which, in turn, is associated with severe liver steatosis in an obesity unit-based sample of women.
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PMID:Obstructive sleep apnoea, glucose tolerance and liver steatosis in obese women. 1769 22

The polycystic ovary syndrome (PCOS) affects 5-10% of women of child-bearing age, and the diagnosis carries with it associated metabolic and cardiovascular risk factors that are likely linked to insulin resistance. Consequently, women affected by PCOS are at significant risk for developing type 2 diabetes mellitus, cardiovascular disease, and obstructive sleep apnea. Aggressive screening for glucose intolerance and cardiovascular risk factors should be performed in all PCOS patients, and, when indicated by symptomatology, affected women should be screened for sleep apnea. Long-term goals of therapy should focus on prevention of these comorbidities.
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PMID:Comorbidities in polycystic ovary syndrome: their relationship to insulin resistance. 1907 70

Sleep profoundly affects metabolic pathways. In healthy subjects, experimental sleep restriction caused insulin resistance (IR) and increased evening cortisol and sympathetic activation. Increased obesity in subjects reporting short sleep duration leads to speculation that, during recent decades, decreased sleeping time in the general population may have contributed to the increasing prevalence of obesity. Causal inference is difficult due to lack of control for confounders and inconsistent evidence of temporal sequence. In the general population, obstructive sleep apnoea (OSA) is associated with glucose intolerance. OSA severity is also associated with the degree of IR. However, OSA at baseline does not seem to significantly predict the development of diabetes. Prevalence of the metabolic syndrome is higher in patients with OSA than in obese subjects without OSA. Treatment with continuous positive airway pressure seems to improve glucose metabolism both in diabetic and nondiabetic OSA but mainly in nonobese subjects. The relative role of obesity and OSA in the pathogenesis of metabolic alterations is still unclear and is intensively studied in clinical and experimental models. In the intermittent hypoxia model in rodents, strong interactions are likely to occur between haemodynamic alterations, systemic inflammation and metabolic changes, modulated by genetic background. Molecular and cellular mechanisms are currently being investigated.
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PMID:Sleep, sleep-disordered breathing and metabolic consequences. 1988 Jun 25

Over the past decade substantial evidence has accumulated implicating disorders of sleep in the pathogenesis of various metabolic abnormalities. This review, which is based on workshop discussions that took place at the 6th annual meeting of the International Sleep Disorders Forum: The Art of Good Sleep 2008 and a systematic literature search, provides a critical analysis of the available evidence implicating sleep disorders such as obstructive sleep apnoea (OSA), insomnia, short or long-term sleep duration and restless legs syndrome as potential risk factors for insulin resistance, glucose intolerance, type 2 diabetes mellitus and the metabolic syndrome. The review also highlights the evidence on whether treatment of specific sleep disorders can decrease metabolic risk. In total, 83 published reports were selected for inclusion. Although several studies show clear associations between sleep disorders and altered glucose metabolism, causal effects and the underlying pathophysiological mechanisms involved have not been fully elucidated. OSA appears to have the strongest association with insulin resistance, glucose intolerance, type 2 diabetes and the metabolic syndrome. There are, however, limited data supporting the hypothesis that effective treatment of sleep disorders, including OSA, has a favourable effect on glucose metabolism. Large randomized trials are thus required to address whether improvement of sleep quality and quantity can curtail excess metabolic risk. Research is also required to elucidate the mechanisms involved and to determine whether the effects of treatment for sleep disorders on glucose metabolism are dependent on the specific patient factors, the type of disorder and the duration of metabolic dysfunction. In conclusion, there is limited evidence on whether sleep disorders alter glucose metabolism and whether treatment can reduce the excess metabolic risk.
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PMID:Do sleep disorders and associated treatments impact glucose metabolism? 2004 48


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